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Musculoskeletal System > Pathology III Bone Tissue > Flashcards

Pathology III Bone Tissue Flashcards

1
Q

Cretinism or “Christ-like”

A

Is one of the disorders of the growth plate

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2
Q

A 3 y/o pt. presents with mental retardation, dwarfism, and a failure of fontanelle closure. The pt. was born with umbilical hernias, coarse facial features, and hypotonic posture. Mother had iodine deficiency while pregnant.

A

Cretinism

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3
Q

Why are the children mentally retarded in cretinism?

A

defective issues in the formation of the neural tube

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4
Q

Why do we used iodinated salt in the US?

A

To prophylax

maternal iodine deficiency leads to cretinism

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5
Q

What do you look for in fontanelle closure?

A

Look at the front of the children’s heads

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6
Q

Which cells are affected in cretinism?

A

Chondrocytes do not follow an orderly progression and there is a failure of ossification

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7
Q

How is cretinism different from achondroplasia?

A

The dwarfs are not mentally retarded in achondroplasia

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8
Q

How is cretinism tx?

A

Many Sx are resolved by administering thyroid hormone

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9
Q

A 9 y/o presents with mental retardation, corneal opacities, hearing defects, cardiac valve disturbances, and DENTAL DEFECTS. What is the mechanism of this disorder?

A

A deposition of glucosaminoglycans in developing bones

MORQUIO SYNDROME

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10
Q

What type of mucopolysacchariodosis is morquio syndrome?

A

Type IV

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11
Q

Compare morquio syndrome to cretinism and achondroplasia

A

A severe form of dwarfism but overall more like cretinism than achondroplasia

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12
Q

A dwarf patient has the head of a typical size with a small body

A

Achondroplastic patient

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13
Q

What causes achondroplasia

A

the arrest of the growth plate

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14
Q

What type of dwarfism is presented in achondroplasia

A

An inheritied dwarfism

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15
Q

What is the most common disease of the growth plate?

A

Achondroplasia

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16
Q

A pt whose heterozygous parents are affected shown sign of dwarfism with shorted limbs

A

Achondroplsia

Autosomal dominant condition
Decrease of paracrine signaling (FGF)
The parents will have 25% change of having normal children

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17
Q

Type I collagen disease

A

Osteogenesis imperfecta or “brittle bone disease”

A defect in the extracellular protein, collegen I

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18
Q

In addition to skeleton, what other sites are affected in osteogenesis imperfecta?

A 
The sites highly rich in type I collagen : 
joints
eyes 
ears 
skin
teeth
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19
Q

Where is the deficiency in type I collagen?

A

Osteoblasts

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20
Q

Type I collagen are mainly present in what?

A

Bone and sclera (fibrocartilage)

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21
Q

Diagnosis of osteogenesis imperfecta

A

Presence of BLUE SCLERA

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22
Q

A Pt. presents with multiple fractures in the lower limbs over the course of a few years. Physical exam reveals blue sclera. The pt. opts for amputation.

A

Osteogenesis imperfecta

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23
Q

What condition, other than osteogenesis imperfecta, can cause blue sclera?

A

Tetracycline overdose- will also cause blue ears

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24
Q

Diseases associated with defects in metabolic pathway

A

Osteopetrosis

25
Q

Why is the juvenile version of osteopetrosis lethal?

A

Because the calvarium gets very thick in this case and causes herniation of the brain through foramen magnum, atlas, axis, and vertebral canals

26
Q

Osteopetrosis

A

marble bone disease (marbles are rocks) and “albers-shonberg disease”

27
Q

What does diffuse skeletal sclerosis mean in osteopetrosis

A

Sclera = means hard
Petro=rock like e.g. petrous part of the temporal bone

The bones are abnormally brittle and fracture like a piece of CHALK

28
Q

What happens to the bones in the body of someone who has osteopetrosis?

A

The rate of synthesis > the rate of degradation

So over time, the bones of the body become very large

29
Q

What is unique about the architecture of the bone in osteopetrosis?

A

Not the way it should be like a trabecular bone (with proper arrangement and collagen deposition)

-Cannot resist tensile forces the way most bone can

30
Q

Osteopetrosis: Autosomal Recessive vs dominant

A

Malignant - recessive
Benign - dominant
serious genetic defects tend to be recessive since people don’t make it to reproductive age

31
Q

4 types of osteopetrosis

A

Infantile malignant form (letal)
Type II carbonic anhydrase deficiency - probably an inability to produce carbonic acid in order to breakdown the bone
Autosomal dominant type I and II

32
Q

3 stages of Paget Disease

A

osteoclast dysfunction

  1. osteolytic stage
  2. mixed osteoclastic-osteoblastic stage
  3. predominant osteoblastic acitivity
33
Q

What age group for paget?

A

Adults!

34
Q

Differentiate osteoporosis from pager’s

A

age of onset!!!!

PAGET starts mid-adulthood

35
Q

What geographical location is paget RARE?

A

asia and africa

36
Q

Which cytokine is a potent osteoclastic stimulator?

A

IL-6

37
Q

Paramyxovirus causes IL-6 to be released and cause what disease?

A

PAGET

38
Q

Chalk-like fx are present in which two diseases?

A

osteopetrosis and PAGET

39
Q

How does Paget become noticeable in clinical setting?

A

incidental
by x-ray - big bones
paget is benign
won’t present with a lot of sx

40
Q

Lab tests that indicate PAGET’s ?

A

increase serum hydroxyproline
increase serum alkaline phosphatase
indicate bone breakdown (initial problem)

41
Q

Anterior bowing

A

shown in pager’s disease because femur is affected

this is different from lateral bowing in rickett’s and osteomalacia

42
Q

A 30 year old patient complains of pain in the leg and presents with anterior bowing

A

paget’s
pain caused by bone overgrowth and compression of nerves
also vessels are compressed and cause ischemia

43
Q

What are the two serious complications of Paget’s ?

A

osteoarthritis
increased risk of malignant osteosarcoma
increased association with arteriovenous malformation

44
Q

Osteosarcoma resulting from Paget’s

A

FIND THE NODULES OF OSTEOSARCOMA AT THE SPINE (doesn’t break the rule of primary osteosarcoma since in this case it is secondary to another disease like paget’s)
look elsewhere in the body to find nodules at above and below the knee
also look for serum levels of hydroxyproline and alkaline phosphatase

45
Q

AV shunting in Paget’s

A

high cardiac output
heart failure
redness over AV shunt on chest

46
Q

Vit D deficiency

A

Rickett’s
Osteomalacia
bone isn’t formed properly because ineffective mineralization of the osteoid secreted by osteoblasts

47
Q

Differentiate Rickett’s from Osteomalacia

A

Rickett’s in KIDS

Osteomalacia in ADULTS

48
Q

Hyperparathyroidism

A

PTH plays a central role in calcium homeostasis by stimulating osteoclasts to increase bone resorption = MOBILIZE CALCIUM

49
Q

The patient has high serum calcium and PTH levels

A

suspect hyperPTH

50
Q

Hypercalcemia

A

cause dementia

51
Q

Vit D synthesis is stimulated by which hormone?

A

PTH

52
Q

a osteoporotic patient is given calcium. the person developed parathyroid tumor, what happens?

A

more PTH released
more calcium in the system
DEMENTIA

53
Q

Iatrogenic dementia

A

from calcium supplement to patients with osteoporosis who develops PTH tumor

54
Q

Osteomyelitis

A

inflammation of bone and marrow

55
Q

A patient infected with s. aureus who inflammation of the bone and marrow

A

pyogenic osteomyelitis
blood-borne
through vasculature

56
Q

A sickle cell patient infected with what agent will have inflammation of the bone and marrow

A

salmonella

pyogenic osteomyelitis

57
Q

A patient infected with TB will develop mycobacterial osteomyelitis

A

POTT’s disease

58
Q

What is pot’s disease

A

mycobacterial osteomyelitis

Musculoskeletal System (27 decks)

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